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Boster Bio mouse bdnf picokine elisa kit
FIGURE 6 Whole-brain <t>BDNF.</t> When normalized to their respective sex controls, males overall exhibited small but significant decreases to BDNF compared to females. Black bars indicate water, and gray bars indicate 10% EtOH. The dashed line indicates 100% RC H2O expression. ‡ significant sex difference at p < .05
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Boster Bio mouse bdnf elisa kit
( A ) Timeline diagram of the experimental procedures. ( B ) Cage setup of the SE and EE housing. ( C ) Immunostaining analyses of <t>BDNF</t> in the hypothalamus of wild-type (WT) mice after 4 weeks of SE and EE housing ( n = 6). TV, third ventricle; * P < 0.05 versus SE mice. Scale bars, 40 μm. DAPI, 4′,6-diamidino-2-phenylindole. ( D ) Typical M-mode images of the hearts were obtained from mice at days 3, 7, and 14 after MI or sham surgery. ( E ) EF, FS, left ventricular ESV, left ventricular EDV, LVESD, and LVEDD were measured using echocardiography at 3, 7, and 14 days after MI or sham surgery ( n = 8 to 9). * P < 0.05 versus SE. Data are expressed as means ± SEM. Data in (C) were analyzed using the Student’s t test. Data in (E) were analyzed using two-way analysis of variance (ANOVA) followed by Bonferroni post hoc analysis.
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Boster Bio mouse bdnf picokinetm elisa kit
Treatment with sPIF restores DYRK1A and <t>BDNF</t> protein levels in the brain of Dp(16)1Yey pups on P6. Evaluation of the DYRK1A protein level in WT pups (vehicle: n = 5; sPIF: n = 5) and Dp(16)1Yey pups (vehicle: n = 3; sPIF: n = 5) ( A ). The brain BDNF protein concentration in WT pups (vehicle: n = 6; sPIF: n = 4) and Dp(16)1Yey pups (vehicle: n = 4; sPIF: n = 6) ( B ). Data are expressed as the mean ± SD and were analyzed in a two-way ANOVA followed by Fisher’s least squares difference test. ** p < 0.01
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Aviva Systems mouse bdnf elisa kit
Figure 3. Effects of morphine treatment, incision and the combination on spinal cord gene expression. Expression patterns of spinal <t>Bdnf</t> and Pdyn on (a) day 1 and (b) day 3 after incision. Expression of Bdnf was higher in morphine-treated plus incision animals one day after surgery. Increased expression changes for Pdyn were observed at both one and three days after incision for all groups, and greater enhancement of expression in the morphine plus incision group at both time points. Error bars: SEM, n ¼ 5/group; *p < 0.05, ***p < 0.001 for comparison with controls and #p < 0.05 for within groups comparisons. Data were analyzed by two-way analysis of variance (ANOVA) followed by Fisher post hoc test for multiple comparisons within each time point.
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Figure 3. Effects of morphine treatment, incision and the combination on spinal cord gene expression. Expression patterns of spinal <t>Bdnf</t> and Pdyn on (a) day 1 and (b) day 3 after incision. Expression of Bdnf was higher in morphine-treated plus incision animals one day after surgery. Increased expression changes for Pdyn were observed at both one and three days after incision for all groups, and greater enhancement of expression in the morphine plus incision group at both time points. Error bars: SEM, n ¼ 5/group; *p < 0.05, ***p < 0.001 for comparison with controls and #p < 0.05 for within groups comparisons. Data were analyzed by two-way analysis of variance (ANOVA) followed by Fisher post hoc test for multiple comparisons within each time point.
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Biosynth Carbosynth mouse bdnf elisa kit
FIGURE 5 | Brain-derived neurotrophic factor <t>(BDNF)</t> protein level in the frontal cortex of mice in control (Con), quetiapine (Que), MK-801 (MK), and MK-801+quetiapine (MK+Que) groups. Quetiapine attenuated the decrease of BDNF level in the frontal cortex of MK-801 mice. n=5 in each group. Mice were treated with chronic quetiapine (10 mg/kg/day, intraperitoneally) for 28 days. From day 22 to 28, 1 h after the administration of quetiapine, the mice were administered MK-801 (2 mg/kg/day, subcutaneously). One day after behavioral testing, the mice were sacrificed for BDNF protein analysis by <t>ELISA.</t> Results are expressed as means ± S.E.M. *P < 0.05 vs. Con, #P < 0.05 vs. MK.
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Boster Bio mouse trkb elisa kit
a Gene ontology (GO) biological processes pathway analysis shows that MIA microglia increase synaptogenic functions while repopulated microglia recover homeostatic functions. Left (red): Top significantly enriched GO biological process terms increased by MIA and decreased by repopulation. Right (purple): Top significantly enriched GO biological process terms decreased by MIA and increased by repopulation. These GO findings were verified using GORILLA. b IPA of genes with differential expression in microglia between MIA versus Saline (RNA-seq data). Pathway analysis reveals MIA-induced upregulation of neuritogenic gene expression, specifically in developmental stages, based on activation z -score. Red denotes pathway activated in E17 MIA microglia. c Genes in “neuritogenesis/formation of cellular protrusions” function. Hierarchal clustering of gene sets based on relative expression values; red: high relative expression, blue: low relative expression. Cluster 1 represents genes increased in adult MIA microglia but reduced in MIA + MG-REP including Ctnnd2, Ncam2, and Ntrk2 . Cluster 2 represents genes increased in immature MIA microglia including Ncam2, Ntn, Ptn and Wnt5a . Cluster3 represents genes decreased in immature MIA microglia including Plau. In situ hybridization (ISH) and immunofluorescence of E17 Saline or MIA offspring in the cortical plate region. d mRNA of cellular protrusion/ neuritogenic genes ( Ctnnd2, Ncam2, Ntn, Ptn, and Wnt5a ) were detected by florescent-labeled antisense cRNA probes (red) but not by scramble cRNA probe (not detected: N.D.), and the sections were immunostained for IBA1 (green) and DAPI (blue). e The number of IBA1 + cells expressing the cellular protrusion/neuritogenic genes were quantified in the cortical plate region. n = (4–5/2) male mice/ litters per molecule for Saline and MIA, n = 3 for scramble control probe. * p < 0.05, ** p < 0.01, ns denotes no significance, by unpaired Student t test. Graphs indicate mean ± s.e.m. <t>ELISA</t> verification of selected RNA-seq molecules: CTNND2 ( f ), NCAM2 ( g ), NTRK2 ( h ), NTN ( i) , PTN ( j ) and WNT5A ( k ) in acutely isolated microglia. MIA increases protein expression of cellular protrusion/neuriotgenic molecules in microglia that were normalized via repopulation. n = (6/4, 6/3, 5/3, 6/3) female mice/litters for P60 Saline + CTRL, MIA + CTRL, Saline + MG-REP and MIA + MG-REP. CTNND2: Prenatal treatment effect, F (1,19) = 157.1, p < 0.0001, Drug effect, F (1,19) = 262.7, p < 0.0001, Interaction effect, F (1,19) = 201, p < 0.0001, NCAM2: Prenatal treatment effect, F (1,19) = 23.76, p = 0.0001, Drug effect, F (1,19) = 26.29, p < 0.0001, Interaction effect, F (1,19) = 17.63, p = 0.0005, NTRK2: Prenatal treatment effect, F (1,18) = 13.99, p = 0.0015, Drug effect, F (1,18) = 12.45, p = 0.0024, Interaction effect, F (1,18) = 0.06203, p = 0.8061, NTN: Prenatal treatment effect, F (1,19) = 0.01669, p = 0.8986, Drug effect, F (1,19) = 0.8, p = 0.3823, Interaction effect, F (1,19) = 6.121, p = 0.0230, PTN: Prenatal treatment effect, F (1,19) = 10.31, p = 0.0046, Drug effect, F (1,19) = 52.02, p < 0.0001, Interaction effect, F (1,19) = 0.002927 p = 0.9574, WNT5A: Prenatal treatment effect, F (1,19) = 5.581, p = 0.0290, Drug effect, F (1,19) = 1.550, p = 0.2282, Interaction effect, F (1,19) = 0.0834 p = 0.7799, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 as determined by 2-way ANOVA (alpha = 0.05) with Tukey’s post-hoc. # p < 0.05 for main effect of MIA. Graphs indicate mean ± s.e.m.
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a Gene ontology (GO) biological processes pathway analysis shows that MIA microglia increase synaptogenic functions while repopulated microglia recover homeostatic functions. Left (red): Top significantly enriched GO biological process terms increased by MIA and decreased by repopulation. Right (purple): Top significantly enriched GO biological process terms decreased by MIA and increased by repopulation. These GO findings were verified using GORILLA. b IPA of genes with differential expression in microglia between MIA versus Saline (RNA-seq data). Pathway analysis reveals MIA-induced upregulation of neuritogenic gene expression, specifically in developmental stages, based on activation z -score. Red denotes pathway activated in E17 MIA microglia. c Genes in “neuritogenesis/formation of cellular protrusions” function. Hierarchal clustering of gene sets based on relative expression values; red: high relative expression, blue: low relative expression. Cluster 1 represents genes increased in adult MIA microglia but reduced in MIA + MG-REP including Ctnnd2, Ncam2, and Ntrk2 . Cluster 2 represents genes increased in immature MIA microglia including Ncam2, Ntn, Ptn and Wnt5a . Cluster3 represents genes decreased in immature MIA microglia including Plau. In situ hybridization (ISH) and immunofluorescence of E17 Saline or MIA offspring in the cortical plate region. d mRNA of cellular protrusion/ neuritogenic genes ( Ctnnd2, Ncam2, Ntn, Ptn, and Wnt5a ) were detected by florescent-labeled antisense cRNA probes (red) but not by scramble cRNA probe (not detected: N.D.), and the sections were immunostained for IBA1 (green) and DAPI (blue). e The number of IBA1 + cells expressing the cellular protrusion/neuritogenic genes were quantified in the cortical plate region. n = (4–5/2) male mice/ litters per molecule for Saline and MIA, n = 3 for scramble control probe. * p < 0.05, ** p < 0.01, ns denotes no significance, by unpaired Student t test. Graphs indicate mean ± s.e.m. <t>ELISA</t> verification of selected RNA-seq molecules: CTNND2 ( f ), NCAM2 ( g ), NTRK2 ( h ), NTN ( i) , PTN ( j ) and WNT5A ( k ) in acutely isolated microglia. MIA increases protein expression of cellular protrusion/neuriotgenic molecules in microglia that were normalized via repopulation. n = (6/4, 6/3, 5/3, 6/3) female mice/litters for P60 Saline + CTRL, MIA + CTRL, Saline + MG-REP and MIA + MG-REP. CTNND2: Prenatal treatment effect, F (1,19) = 157.1, p < 0.0001, Drug effect, F (1,19) = 262.7, p < 0.0001, Interaction effect, F (1,19) = 201, p < 0.0001, NCAM2: Prenatal treatment effect, F (1,19) = 23.76, p = 0.0001, Drug effect, F (1,19) = 26.29, p < 0.0001, Interaction effect, F (1,19) = 17.63, p = 0.0005, NTRK2: Prenatal treatment effect, F (1,18) = 13.99, p = 0.0015, Drug effect, F (1,18) = 12.45, p = 0.0024, Interaction effect, F (1,18) = 0.06203, p = 0.8061, NTN: Prenatal treatment effect, F (1,19) = 0.01669, p = 0.8986, Drug effect, F (1,19) = 0.8, p = 0.3823, Interaction effect, F (1,19) = 6.121, p = 0.0230, PTN: Prenatal treatment effect, F (1,19) = 10.31, p = 0.0046, Drug effect, F (1,19) = 52.02, p < 0.0001, Interaction effect, F (1,19) = 0.002927 p = 0.9574, WNT5A: Prenatal treatment effect, F (1,19) = 5.581, p = 0.0290, Drug effect, F (1,19) = 1.550, p = 0.2282, Interaction effect, F (1,19) = 0.0834 p = 0.7799, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 as determined by 2-way ANOVA (alpha = 0.05) with Tukey’s post-hoc. # p < 0.05 for main effect of MIA. Graphs indicate mean ± s.e.m.
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MultiSciences Biotech Co Ltd mouse bdnf elisa kit
a Gene ontology (GO) biological processes pathway analysis shows that MIA microglia increase synaptogenic functions while repopulated microglia recover homeostatic functions. Left (red): Top significantly enriched GO biological process terms increased by MIA and decreased by repopulation. Right (purple): Top significantly enriched GO biological process terms decreased by MIA and increased by repopulation. These GO findings were verified using GORILLA. b IPA of genes with differential expression in microglia between MIA versus Saline (RNA-seq data). Pathway analysis reveals MIA-induced upregulation of neuritogenic gene expression, specifically in developmental stages, based on activation z -score. Red denotes pathway activated in E17 MIA microglia. c Genes in “neuritogenesis/formation of cellular protrusions” function. Hierarchal clustering of gene sets based on relative expression values; red: high relative expression, blue: low relative expression. Cluster 1 represents genes increased in adult MIA microglia but reduced in MIA + MG-REP including Ctnnd2, Ncam2, and Ntrk2 . Cluster 2 represents genes increased in immature MIA microglia including Ncam2, Ntn, Ptn and Wnt5a . Cluster3 represents genes decreased in immature MIA microglia including Plau. In situ hybridization (ISH) and immunofluorescence of E17 Saline or MIA offspring in the cortical plate region. d mRNA of cellular protrusion/ neuritogenic genes ( Ctnnd2, Ncam2, Ntn, Ptn, and Wnt5a ) were detected by florescent-labeled antisense cRNA probes (red) but not by scramble cRNA probe (not detected: N.D.), and the sections were immunostained for IBA1 (green) and DAPI (blue). e The number of IBA1 + cells expressing the cellular protrusion/neuritogenic genes were quantified in the cortical plate region. n = (4–5/2) male mice/ litters per molecule for Saline and MIA, n = 3 for scramble control probe. * p < 0.05, ** p < 0.01, ns denotes no significance, by unpaired Student t test. Graphs indicate mean ± s.e.m. <t>ELISA</t> verification of selected RNA-seq molecules: CTNND2 ( f ), NCAM2 ( g ), NTRK2 ( h ), NTN ( i) , PTN ( j ) and WNT5A ( k ) in acutely isolated microglia. MIA increases protein expression of cellular protrusion/neuriotgenic molecules in microglia that were normalized via repopulation. n = (6/4, 6/3, 5/3, 6/3) female mice/litters for P60 Saline + CTRL, MIA + CTRL, Saline + MG-REP and MIA + MG-REP. CTNND2: Prenatal treatment effect, F (1,19) = 157.1, p < 0.0001, Drug effect, F (1,19) = 262.7, p < 0.0001, Interaction effect, F (1,19) = 201, p < 0.0001, NCAM2: Prenatal treatment effect, F (1,19) = 23.76, p = 0.0001, Drug effect, F (1,19) = 26.29, p < 0.0001, Interaction effect, F (1,19) = 17.63, p = 0.0005, NTRK2: Prenatal treatment effect, F (1,18) = 13.99, p = 0.0015, Drug effect, F (1,18) = 12.45, p = 0.0024, Interaction effect, F (1,18) = 0.06203, p = 0.8061, NTN: Prenatal treatment effect, F (1,19) = 0.01669, p = 0.8986, Drug effect, F (1,19) = 0.8, p = 0.3823, Interaction effect, F (1,19) = 6.121, p = 0.0230, PTN: Prenatal treatment effect, F (1,19) = 10.31, p = 0.0046, Drug effect, F (1,19) = 52.02, p < 0.0001, Interaction effect, F (1,19) = 0.002927 p = 0.9574, WNT5A: Prenatal treatment effect, F (1,19) = 5.581, p = 0.0290, Drug effect, F (1,19) = 1.550, p = 0.2282, Interaction effect, F (1,19) = 0.0834 p = 0.7799, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 as determined by 2-way ANOVA (alpha = 0.05) with Tukey’s post-hoc. # p < 0.05 for main effect of MIA. Graphs indicate mean ± s.e.m.
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a Gene ontology (GO) biological processes pathway analysis shows that MIA microglia increase synaptogenic functions while repopulated microglia recover homeostatic functions. Left (red): Top significantly enriched GO biological process terms increased by MIA and decreased by repopulation. Right (purple): Top significantly enriched GO biological process terms decreased by MIA and increased by repopulation. These GO findings were verified using GORILLA. b IPA of genes with differential expression in microglia between MIA versus Saline (RNA-seq data). Pathway analysis reveals MIA-induced upregulation of neuritogenic gene expression, specifically in developmental stages, based on activation z -score. Red denotes pathway activated in E17 MIA microglia. c Genes in “neuritogenesis/formation of cellular protrusions” function. Hierarchal clustering of gene sets based on relative expression values; red: high relative expression, blue: low relative expression. Cluster 1 represents genes increased in adult MIA microglia but reduced in MIA + MG-REP including Ctnnd2, Ncam2, and Ntrk2 . Cluster 2 represents genes increased in immature MIA microglia including Ncam2, Ntn, Ptn and Wnt5a . Cluster3 represents genes decreased in immature MIA microglia including Plau. In situ hybridization (ISH) and immunofluorescence of E17 Saline or MIA offspring in the cortical plate region. d mRNA of cellular protrusion/ neuritogenic genes ( Ctnnd2, Ncam2, Ntn, Ptn, and Wnt5a ) were detected by florescent-labeled antisense cRNA probes (red) but not by scramble cRNA probe (not detected: N.D.), and the sections were immunostained for IBA1 (green) and DAPI (blue). e The number of IBA1 + cells expressing the cellular protrusion/neuritogenic genes were quantified in the cortical plate region. n = (4–5/2) male mice/ litters per molecule for Saline and MIA, n = 3 for scramble control probe. * p < 0.05, ** p < 0.01, ns denotes no significance, by unpaired Student t test. Graphs indicate mean ± s.e.m. <t>ELISA</t> verification of selected RNA-seq molecules: CTNND2 ( f ), NCAM2 ( g ), NTRK2 ( h ), NTN ( i) , PTN ( j ) and WNT5A ( k ) in acutely isolated microglia. MIA increases protein expression of cellular protrusion/neuriotgenic molecules in microglia that were normalized via repopulation. n = (6/4, 6/3, 5/3, 6/3) female mice/litters for P60 Saline + CTRL, MIA + CTRL, Saline + MG-REP and MIA + MG-REP. CTNND2: Prenatal treatment effect, F (1,19) = 157.1, p < 0.0001, Drug effect, F (1,19) = 262.7, p < 0.0001, Interaction effect, F (1,19) = 201, p < 0.0001, NCAM2: Prenatal treatment effect, F (1,19) = 23.76, p = 0.0001, Drug effect, F (1,19) = 26.29, p < 0.0001, Interaction effect, F (1,19) = 17.63, p = 0.0005, NTRK2: Prenatal treatment effect, F (1,18) = 13.99, p = 0.0015, Drug effect, F (1,18) = 12.45, p = 0.0024, Interaction effect, F (1,18) = 0.06203, p = 0.8061, NTN: Prenatal treatment effect, F (1,19) = 0.01669, p = 0.8986, Drug effect, F (1,19) = 0.8, p = 0.3823, Interaction effect, F (1,19) = 6.121, p = 0.0230, PTN: Prenatal treatment effect, F (1,19) = 10.31, p = 0.0046, Drug effect, F (1,19) = 52.02, p < 0.0001, Interaction effect, F (1,19) = 0.002927 p = 0.9574, WNT5A: Prenatal treatment effect, F (1,19) = 5.581, p = 0.0290, Drug effect, F (1,19) = 1.550, p = 0.2282, Interaction effect, F (1,19) = 0.0834 p = 0.7799, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 as determined by 2-way ANOVA (alpha = 0.05) with Tukey’s post-hoc. # p < 0.05 for main effect of MIA. Graphs indicate mean ± s.e.m.
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Image Search Results


FIGURE 6 Whole-brain BDNF. When normalized to their respective sex controls, males overall exhibited small but significant decreases to BDNF compared to females. Black bars indicate water, and gray bars indicate 10% EtOH. The dashed line indicates 100% RC H2O expression. ‡ significant sex difference at p < .05

Journal: Brain and behavior

Article Title: The behavioral and physiological effects of high-fat diet and alcohol consumption: Sex differences in C57BL6/J mice.

doi: 10.1002/brb3.708

Figure Lengend Snippet: FIGURE 6 Whole-brain BDNF. When normalized to their respective sex controls, males overall exhibited small but significant decreases to BDNF compared to females. Black bars indicate water, and gray bars indicate 10% EtOH. The dashed line indicates 100% RC H2O expression. ‡ significant sex difference at p < .05

Article Snippet: A low target concentration (working dilution 1:2) of sample and sample diluent buffer was created and then used in a BDNF ELISA (Mouse BDNF PicoKine ELISA Kit, Boster Biological Technology Co., Pleasanton, CA, USA).

Techniques: Expressing

( A ) Timeline diagram of the experimental procedures. ( B ) Cage setup of the SE and EE housing. ( C ) Immunostaining analyses of BDNF in the hypothalamus of wild-type (WT) mice after 4 weeks of SE and EE housing ( n = 6). TV, third ventricle; * P < 0.05 versus SE mice. Scale bars, 40 μm. DAPI, 4′,6-diamidino-2-phenylindole. ( D ) Typical M-mode images of the hearts were obtained from mice at days 3, 7, and 14 after MI or sham surgery. ( E ) EF, FS, left ventricular ESV, left ventricular EDV, LVESD, and LVEDD were measured using echocardiography at 3, 7, and 14 days after MI or sham surgery ( n = 8 to 9). * P < 0.05 versus SE. Data are expressed as means ± SEM. Data in (C) were analyzed using the Student’s t test. Data in (E) were analyzed using two-way analysis of variance (ANOVA) followed by Bonferroni post hoc analysis.

Journal: Science Advances

Article Title: Environmental eustress improves postinfarction cardiac repair via enhancing cardiac macrophage survival

doi: 10.1126/sciadv.abm3436

Figure Lengend Snippet: ( A ) Timeline diagram of the experimental procedures. ( B ) Cage setup of the SE and EE housing. ( C ) Immunostaining analyses of BDNF in the hypothalamus of wild-type (WT) mice after 4 weeks of SE and EE housing ( n = 6). TV, third ventricle; * P < 0.05 versus SE mice. Scale bars, 40 μm. DAPI, 4′,6-diamidino-2-phenylindole. ( D ) Typical M-mode images of the hearts were obtained from mice at days 3, 7, and 14 after MI or sham surgery. ( E ) EF, FS, left ventricular ESV, left ventricular EDV, LVESD, and LVEDD were measured using echocardiography at 3, 7, and 14 days after MI or sham surgery ( n = 8 to 9). * P < 0.05 versus SE. Data are expressed as means ± SEM. Data in (C) were analyzed using the Student’s t test. Data in (E) were analyzed using two-way analysis of variance (ANOVA) followed by Bonferroni post hoc analysis.

Article Snippet: Plasma BDNF levels were then determined using the Mouse BDNF ELISA Kit (Boster Biological Technology Ltd., Wuhan, China), according to the manufacturer’s instructions.

Techniques: Immunostaining

( A ) mRNA expression of agouti-related peptide ( Agrp ), Bdnf , leptin receptor ( Lepr ), neuropeptide Y ( Npy ), neurotrophic receptor tyrosine kinase 2 ( Ntrk2 ), serum/glucocorticoid-regulated kinase1 ( Sgk1 ), and nerve growth factor inducible ( Vgf ) in hypothalamus obtained from SE and EE mice at day 7 after MI ( n = 6). * P < 0.05 versus SE. ( B ) mRNA expression of BDNF in bone marrow (BM), spleen, heart, and hypothalamus collected from SE and EE mice at day 7 after MI ( n = 6). * P < 0.05 versus SE. ( C ) The BDNF content in plasma of SE- and EE-housed mice at day 14 after MI or sham operation. * P < 0.05 versus SE and # P < 0.05 versus sham. ( D ) Western blot analyses of BDNF and TrkB expression in the infarct tissues at day 14 after MI ( n = 6). * P < 0.05 versus MI-SE. ( E ) TrkB mRNA expression in cardiomyocytes (CMs), fibroblasts (Fb), endothelial cells (ECs), and CCR2 − MHCII low macrophages sorted from the hearts at day 7 after MI ( n = 6). * P < 0.05 versus MI-SE. ( F ) Immunostaining analyses of Arg-1, cardiac troponin I (TNNI3), and TrkB on infarct sections collected at 14 days after MI. Scale bars, 20 μm. ( G ) Immunostaining of p-ERK1/2 and p-AKT in CCR2 − MHCII low macrophages sorted from infarcted hearts. Scale bars, 50 μm. ( H ) Immunostaining of Bcl-2 and Bax in CCR2 − MHCII low macrophages sorted from the infarcted hearts. Scale bars, 50 μm. ( I ) Mechanism of EE-induced cardioprotective effect in mice after MI.Data are expressed as means ± SEM. Data in (C) were analyzed using two-way ANOVA followed by Bonferroni post hoc analysis. Data in (A), (B), (D), and (E) were analyzed using Student’s t test.

Journal: Science Advances

Article Title: Environmental eustress improves postinfarction cardiac repair via enhancing cardiac macrophage survival

doi: 10.1126/sciadv.abm3436

Figure Lengend Snippet: ( A ) mRNA expression of agouti-related peptide ( Agrp ), Bdnf , leptin receptor ( Lepr ), neuropeptide Y ( Npy ), neurotrophic receptor tyrosine kinase 2 ( Ntrk2 ), serum/glucocorticoid-regulated kinase1 ( Sgk1 ), and nerve growth factor inducible ( Vgf ) in hypothalamus obtained from SE and EE mice at day 7 after MI ( n = 6). * P < 0.05 versus SE. ( B ) mRNA expression of BDNF in bone marrow (BM), spleen, heart, and hypothalamus collected from SE and EE mice at day 7 after MI ( n = 6). * P < 0.05 versus SE. ( C ) The BDNF content in plasma of SE- and EE-housed mice at day 14 after MI or sham operation. * P < 0.05 versus SE and # P < 0.05 versus sham. ( D ) Western blot analyses of BDNF and TrkB expression in the infarct tissues at day 14 after MI ( n = 6). * P < 0.05 versus MI-SE. ( E ) TrkB mRNA expression in cardiomyocytes (CMs), fibroblasts (Fb), endothelial cells (ECs), and CCR2 − MHCII low macrophages sorted from the hearts at day 7 after MI ( n = 6). * P < 0.05 versus MI-SE. ( F ) Immunostaining analyses of Arg-1, cardiac troponin I (TNNI3), and TrkB on infarct sections collected at 14 days after MI. Scale bars, 20 μm. ( G ) Immunostaining of p-ERK1/2 and p-AKT in CCR2 − MHCII low macrophages sorted from infarcted hearts. Scale bars, 50 μm. ( H ) Immunostaining of Bcl-2 and Bax in CCR2 − MHCII low macrophages sorted from the infarcted hearts. Scale bars, 50 μm. ( I ) Mechanism of EE-induced cardioprotective effect in mice after MI.Data are expressed as means ± SEM. Data in (C) were analyzed using two-way ANOVA followed by Bonferroni post hoc analysis. Data in (A), (B), (D), and (E) were analyzed using Student’s t test.

Article Snippet: Plasma BDNF levels were then determined using the Mouse BDNF ELISA Kit (Boster Biological Technology Ltd., Wuhan, China), according to the manufacturer’s instructions.

Techniques: Expressing, Clinical Proteomics, Western Blot, Immunostaining

( A ) Timeline diagram of the experimental procedures. ( B ) Western blot analysis of BDNF expression in the hypothalamus between HBKD and control mice 4 weeks after the virus injection ( n = 6). * P < 0.05 versus control. ( C ) The BDNF content in plasma of HBKD and control mice at day 14 after MI after SE and EE housing. # P < 0.05 versus SE-MI. * P < 0.05 versus control. ( D ) Echocardiographic analysis of EF value of HBKD and control mice at day 14 after MI after SE and EE housing ( n = 8). # P < 0.05 versus SE-MI and * P < 0.05 versus control. ( E ) Masson’s staining of cardiac tissue obtained from HBKD and control mice at day 14 after MI after SE and EE housing. Quantitative analysis of infarct size and wall thickness ( n = 8). # P < 0.05 versus SE-MI. * P < 0.05 versus control. ( F and G ) Immunostaining analyses of CD31, α-SMA, collagen I, and collagen III on infarct sections collected at 14 days after MI. Scale bars, 50 μm (for CD31) and 20 μm (for α-SMA, collagen I, and collagen III). ( H ) Representative Western blot analyses of collagen I, α-SMA, VEGF, and CD31 expression in the infarct tissues at day 14 after MI ( n = 6). ( I ) mRNA expression of α-SMA , Col1a1 , and Col3a1 in scar tissues at day 14 after MI. # P < 0.05 versus SE-MI. * P < 0.05 versus control. ( J ) Gating strategy and quantification of CCR2 − MHCII low macrophages in the hearts of HBKD and control mice after MI ( n = 6). # P < 0.05 versus SE-MI. * P < 0.05 versus control.

Journal: Science Advances

Article Title: Environmental eustress improves postinfarction cardiac repair via enhancing cardiac macrophage survival

doi: 10.1126/sciadv.abm3436

Figure Lengend Snippet: ( A ) Timeline diagram of the experimental procedures. ( B ) Western blot analysis of BDNF expression in the hypothalamus between HBKD and control mice 4 weeks after the virus injection ( n = 6). * P < 0.05 versus control. ( C ) The BDNF content in plasma of HBKD and control mice at day 14 after MI after SE and EE housing. # P < 0.05 versus SE-MI. * P < 0.05 versus control. ( D ) Echocardiographic analysis of EF value of HBKD and control mice at day 14 after MI after SE and EE housing ( n = 8). # P < 0.05 versus SE-MI and * P < 0.05 versus control. ( E ) Masson’s staining of cardiac tissue obtained from HBKD and control mice at day 14 after MI after SE and EE housing. Quantitative analysis of infarct size and wall thickness ( n = 8). # P < 0.05 versus SE-MI. * P < 0.05 versus control. ( F and G ) Immunostaining analyses of CD31, α-SMA, collagen I, and collagen III on infarct sections collected at 14 days after MI. Scale bars, 50 μm (for CD31) and 20 μm (for α-SMA, collagen I, and collagen III). ( H ) Representative Western blot analyses of collagen I, α-SMA, VEGF, and CD31 expression in the infarct tissues at day 14 after MI ( n = 6). ( I ) mRNA expression of α-SMA , Col1a1 , and Col3a1 in scar tissues at day 14 after MI. # P < 0.05 versus SE-MI. * P < 0.05 versus control. ( J ) Gating strategy and quantification of CCR2 − MHCII low macrophages in the hearts of HBKD and control mice after MI ( n = 6). # P < 0.05 versus SE-MI. * P < 0.05 versus control.

Article Snippet: Plasma BDNF levels were then determined using the Mouse BDNF ELISA Kit (Boster Biological Technology Ltd., Wuhan, China), according to the manufacturer’s instructions.

Techniques: Western Blot, Expressing, Control, Virus, Injection, Clinical Proteomics, Staining, Immunostaining

Treatment with sPIF restores DYRK1A and BDNF protein levels in the brain of Dp(16)1Yey pups on P6. Evaluation of the DYRK1A protein level in WT pups (vehicle: n = 5; sPIF: n = 5) and Dp(16)1Yey pups (vehicle: n = 3; sPIF: n = 5) ( A ). The brain BDNF protein concentration in WT pups (vehicle: n = 6; sPIF: n = 4) and Dp(16)1Yey pups (vehicle: n = 4; sPIF: n = 6) ( B ). Data are expressed as the mean ± SD and were analyzed in a two-way ANOVA followed by Fisher’s least squares difference test. ** p < 0.01

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Prenatal treatment with preimplantation factor improves early postnatal neurogenesis and cognitive impairments in a mouse model of Down syndrome

doi: 10.1007/s00018-024-05245-9

Figure Lengend Snippet: Treatment with sPIF restores DYRK1A and BDNF protein levels in the brain of Dp(16)1Yey pups on P6. Evaluation of the DYRK1A protein level in WT pups (vehicle: n = 5; sPIF: n = 5) and Dp(16)1Yey pups (vehicle: n = 3; sPIF: n = 5) ( A ). The brain BDNF protein concentration in WT pups (vehicle: n = 6; sPIF: n = 4) and Dp(16)1Yey pups (vehicle: n = 4; sPIF: n = 6) ( B ). Data are expressed as the mean ± SD and were analyzed in a two-way ANOVA followed by Fisher’s least squares difference test. ** p < 0.01

Article Snippet: The levels of brain-derived neurotrophic factor (BDNF) in brain lysates were measured with a mouse BDNF PicokineTM ELISA kit (Boster).

Techniques: Protein Concentration

Figure 3. Effects of morphine treatment, incision and the combination on spinal cord gene expression. Expression patterns of spinal Bdnf and Pdyn on (a) day 1 and (b) day 3 after incision. Expression of Bdnf was higher in morphine-treated plus incision animals one day after surgery. Increased expression changes for Pdyn were observed at both one and three days after incision for all groups, and greater enhancement of expression in the morphine plus incision group at both time points. Error bars: SEM, n ¼ 5/group; *p < 0.05, ***p < 0.001 for comparison with controls and #p < 0.05 for within groups comparisons. Data were analyzed by two-way analysis of variance (ANOVA) followed by Fisher post hoc test for multiple comparisons within each time point.

Journal: Molecular pain

Article Title: Epigenetic regulation of spinal cord gene expression contributes to enhanced postoperative pain and analgesic tolerance subsequent to continuous opioid exposure.

doi: 10.1177/1744806916641950

Figure Lengend Snippet: Figure 3. Effects of morphine treatment, incision and the combination on spinal cord gene expression. Expression patterns of spinal Bdnf and Pdyn on (a) day 1 and (b) day 3 after incision. Expression of Bdnf was higher in morphine-treated plus incision animals one day after surgery. Increased expression changes for Pdyn were observed at both one and three days after incision for all groups, and greater enhancement of expression in the morphine plus incision group at both time points. Error bars: SEM, n ¼ 5/group; *p < 0.05, ***p < 0.001 for comparison with controls and #p < 0.05 for within groups comparisons. Data were analyzed by two-way analysis of variance (ANOVA) followed by Fisher post hoc test for multiple comparisons within each time point.

Article Snippet: BDNF concentrations were measured in duplicate by using mouse BDNF ELISA kit (Gen Way Biotech), and the dynorphin levels were assayed in duplicate by using Dynorphin EIA kit (Phoenix Pharmaceuticals) according to the manufacturer’s instructions.

Techniques: Gene Expression, Expressing, Comparison

Figure 4. Epigenetic effects of morphine treatment, incision and the combination on spinal Bdnf and Pdyn expression. Chromatin immunoprecipitation (ChIP) assays done on lumbar spinal tissue (a) day 1 and (b) day 3 after incision. ChIP assays showed that promoter regions of Bdnf and Pdyn were more strongly associated with aceH3K9 on day 1 after incision in morphine-treated group compared with morphine or incision alone groups. Error bars: SEM, n ¼ 5–6/group; *p < 0.05, ***p < 0.001 for comparison with controls and #p < 0.05, ##p < 0.01 for within groups comparisons. Data were analyzed by two-way analysis of variance (ANOVA) followed by Fisher post hoc test for multiple comparisons within each time point.

Journal: Molecular pain

Article Title: Epigenetic regulation of spinal cord gene expression contributes to enhanced postoperative pain and analgesic tolerance subsequent to continuous opioid exposure.

doi: 10.1177/1744806916641950

Figure Lengend Snippet: Figure 4. Epigenetic effects of morphine treatment, incision and the combination on spinal Bdnf and Pdyn expression. Chromatin immunoprecipitation (ChIP) assays done on lumbar spinal tissue (a) day 1 and (b) day 3 after incision. ChIP assays showed that promoter regions of Bdnf and Pdyn were more strongly associated with aceH3K9 on day 1 after incision in morphine-treated group compared with morphine or incision alone groups. Error bars: SEM, n ¼ 5–6/group; *p < 0.05, ***p < 0.001 for comparison with controls and #p < 0.05, ##p < 0.01 for within groups comparisons. Data were analyzed by two-way analysis of variance (ANOVA) followed by Fisher post hoc test for multiple comparisons within each time point.

Article Snippet: BDNF concentrations were measured in duplicate by using mouse BDNF ELISA kit (Gen Way Biotech), and the dynorphin levels were assayed in duplicate by using Dynorphin EIA kit (Phoenix Pharmaceuticals) according to the manufacturer’s instructions.

Techniques: Expressing, Chromatin Immunoprecipitation, Comparison

Figure 5. Effects of chronic morphine treatment and incision on spinal cord BDNF and dynorphin protein levels. Enzyme immunoassay (ELISA) for BDNF and dynorphin protein levels in lumbar spinal cord segments were done to determine the time course of the elevated proteins after incision in mice previously exposed to morphine. (a) BDNF levels were elevated on days 1 and 3 but return to baseline values by day 6 after incision. (b) Dynorphin levels remain persistently elevated up to day 6 after incision. Error bars: SEM, n ¼ 6/group, *p < 0.05 and **p < 0.01 for comparison with baseline. Data were analyzed by one-way ANOVA followed by Fisher post hoc test multiple com- parisons tests.

Journal: Molecular pain

Article Title: Epigenetic regulation of spinal cord gene expression contributes to enhanced postoperative pain and analgesic tolerance subsequent to continuous opioid exposure.

doi: 10.1177/1744806916641950

Figure Lengend Snippet: Figure 5. Effects of chronic morphine treatment and incision on spinal cord BDNF and dynorphin protein levels. Enzyme immunoassay (ELISA) for BDNF and dynorphin protein levels in lumbar spinal cord segments were done to determine the time course of the elevated proteins after incision in mice previously exposed to morphine. (a) BDNF levels were elevated on days 1 and 3 but return to baseline values by day 6 after incision. (b) Dynorphin levels remain persistently elevated up to day 6 after incision. Error bars: SEM, n ¼ 6/group, *p < 0.05 and **p < 0.01 for comparison with baseline. Data were analyzed by one-way ANOVA followed by Fisher post hoc test multiple com- parisons tests.

Article Snippet: BDNF concentrations were measured in duplicate by using mouse BDNF ELISA kit (Gen Way Biotech), and the dynorphin levels were assayed in duplicate by using Dynorphin EIA kit (Phoenix Pharmaceuticals) according to the manufacturer’s instructions.

Techniques: Enzyme-linked Immunosorbent Assay, Comparison

Figure 6. Effects of selective inhibition of spinal BDNF and dynorphin signaling. (a) Effects of selective antagonists of the tropomyosin- receptor-kinase (TrkB) and k-opioid receptors, ANA-12 and nor-BNI, respectively. Both drugs reduced hyperalgesia given on day 1 or 3 after surgery compared to vehicle treatment. (b) The administration of ANA-12 or nor-BNI attenuated the reduced morphine analgesic efficacy on day 1, but only nor-BNI was effective on day 3 after surgery in opioid-exposed group. Error bars: SEM, n ¼ 6/group, *p < 0.05, **p < 0.01 and ***p < 0.001 for comparison between treatments for each time point. Data for each time point were analyzed by one-way ANOVA followed by Sidak multiple comparisons tests.

Journal: Molecular pain

Article Title: Epigenetic regulation of spinal cord gene expression contributes to enhanced postoperative pain and analgesic tolerance subsequent to continuous opioid exposure.

doi: 10.1177/1744806916641950

Figure Lengend Snippet: Figure 6. Effects of selective inhibition of spinal BDNF and dynorphin signaling. (a) Effects of selective antagonists of the tropomyosin- receptor-kinase (TrkB) and k-opioid receptors, ANA-12 and nor-BNI, respectively. Both drugs reduced hyperalgesia given on day 1 or 3 after surgery compared to vehicle treatment. (b) The administration of ANA-12 or nor-BNI attenuated the reduced morphine analgesic efficacy on day 1, but only nor-BNI was effective on day 3 after surgery in opioid-exposed group. Error bars: SEM, n ¼ 6/group, *p < 0.05, **p < 0.01 and ***p < 0.001 for comparison between treatments for each time point. Data for each time point were analyzed by one-way ANOVA followed by Sidak multiple comparisons tests.

Article Snippet: BDNF concentrations were measured in duplicate by using mouse BDNF ELISA kit (Gen Way Biotech), and the dynorphin levels were assayed in duplicate by using Dynorphin EIA kit (Phoenix Pharmaceuticals) according to the manufacturer’s instructions.

Techniques: Inhibition, Comparison

FIGURE 5 | Brain-derived neurotrophic factor (BDNF) protein level in the frontal cortex of mice in control (Con), quetiapine (Que), MK-801 (MK), and MK-801+quetiapine (MK+Que) groups. Quetiapine attenuated the decrease of BDNF level in the frontal cortex of MK-801 mice. n=5 in each group. Mice were treated with chronic quetiapine (10 mg/kg/day, intraperitoneally) for 28 days. From day 22 to 28, 1 h after the administration of quetiapine, the mice were administered MK-801 (2 mg/kg/day, subcutaneously). One day after behavioral testing, the mice were sacrificed for BDNF protein analysis by ELISA. Results are expressed as means ± S.E.M. *P < 0.05 vs. Con, #P < 0.05 vs. MK.

Journal: Frontiers in psychiatry

Article Title: Quetiapine Attenuates Schizophrenia-Like Behaviors and Demyelination in a MK-801-Induced Mouse Model of Schizophrenia.

doi: 10.3389/fpsyt.2020.00843

Figure Lengend Snippet: FIGURE 5 | Brain-derived neurotrophic factor (BDNF) protein level in the frontal cortex of mice in control (Con), quetiapine (Que), MK-801 (MK), and MK-801+quetiapine (MK+Que) groups. Quetiapine attenuated the decrease of BDNF level in the frontal cortex of MK-801 mice. n=5 in each group. Mice were treated with chronic quetiapine (10 mg/kg/day, intraperitoneally) for 28 days. From day 22 to 28, 1 h after the administration of quetiapine, the mice were administered MK-801 (2 mg/kg/day, subcutaneously). One day after behavioral testing, the mice were sacrificed for BDNF protein analysis by ELISA. Results are expressed as means ± S.E.M. *P < 0.05 vs. Con, #P < 0.05 vs. MK.

Article Snippet: The level of BDNF was quantified using a commercial Mouse BDNF ELISA kit (Fitzgerald Industries International, North Acton, MA) according to the manufacturer’s protocol.

Techniques: Derivative Assay, Control, Enzyme-linked Immunosorbent Assay

a Gene ontology (GO) biological processes pathway analysis shows that MIA microglia increase synaptogenic functions while repopulated microglia recover homeostatic functions. Left (red): Top significantly enriched GO biological process terms increased by MIA and decreased by repopulation. Right (purple): Top significantly enriched GO biological process terms decreased by MIA and increased by repopulation. These GO findings were verified using GORILLA. b IPA of genes with differential expression in microglia between MIA versus Saline (RNA-seq data). Pathway analysis reveals MIA-induced upregulation of neuritogenic gene expression, specifically in developmental stages, based on activation z -score. Red denotes pathway activated in E17 MIA microglia. c Genes in “neuritogenesis/formation of cellular protrusions” function. Hierarchal clustering of gene sets based on relative expression values; red: high relative expression, blue: low relative expression. Cluster 1 represents genes increased in adult MIA microglia but reduced in MIA + MG-REP including Ctnnd2, Ncam2, and Ntrk2 . Cluster 2 represents genes increased in immature MIA microglia including Ncam2, Ntn, Ptn and Wnt5a . Cluster3 represents genes decreased in immature MIA microglia including Plau. In situ hybridization (ISH) and immunofluorescence of E17 Saline or MIA offspring in the cortical plate region. d mRNA of cellular protrusion/ neuritogenic genes ( Ctnnd2, Ncam2, Ntn, Ptn, and Wnt5a ) were detected by florescent-labeled antisense cRNA probes (red) but not by scramble cRNA probe (not detected: N.D.), and the sections were immunostained for IBA1 (green) and DAPI (blue). e The number of IBA1 + cells expressing the cellular protrusion/neuritogenic genes were quantified in the cortical plate region. n = (4–5/2) male mice/ litters per molecule for Saline and MIA, n = 3 for scramble control probe. * p < 0.05, ** p < 0.01, ns denotes no significance, by unpaired Student t test. Graphs indicate mean ± s.e.m. ELISA verification of selected RNA-seq molecules: CTNND2 ( f ), NCAM2 ( g ), NTRK2 ( h ), NTN ( i) , PTN ( j ) and WNT5A ( k ) in acutely isolated microglia. MIA increases protein expression of cellular protrusion/neuriotgenic molecules in microglia that were normalized via repopulation. n = (6/4, 6/3, 5/3, 6/3) female mice/litters for P60 Saline + CTRL, MIA + CTRL, Saline + MG-REP and MIA + MG-REP. CTNND2: Prenatal treatment effect, F (1,19) = 157.1, p < 0.0001, Drug effect, F (1,19) = 262.7, p < 0.0001, Interaction effect, F (1,19) = 201, p < 0.0001, NCAM2: Prenatal treatment effect, F (1,19) = 23.76, p = 0.0001, Drug effect, F (1,19) = 26.29, p < 0.0001, Interaction effect, F (1,19) = 17.63, p = 0.0005, NTRK2: Prenatal treatment effect, F (1,18) = 13.99, p = 0.0015, Drug effect, F (1,18) = 12.45, p = 0.0024, Interaction effect, F (1,18) = 0.06203, p = 0.8061, NTN: Prenatal treatment effect, F (1,19) = 0.01669, p = 0.8986, Drug effect, F (1,19) = 0.8, p = 0.3823, Interaction effect, F (1,19) = 6.121, p = 0.0230, PTN: Prenatal treatment effect, F (1,19) = 10.31, p = 0.0046, Drug effect, F (1,19) = 52.02, p < 0.0001, Interaction effect, F (1,19) = 0.002927 p = 0.9574, WNT5A: Prenatal treatment effect, F (1,19) = 5.581, p = 0.0290, Drug effect, F (1,19) = 1.550, p = 0.2282, Interaction effect, F (1,19) = 0.0834 p = 0.7799, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 as determined by 2-way ANOVA (alpha = 0.05) with Tukey’s post-hoc. # p < 0.05 for main effect of MIA. Graphs indicate mean ± s.e.m.

Journal: Molecular Psychiatry

Article Title: Inhibition of colony stimulating factor 1 receptor corrects maternal inflammation-induced microglial and synaptic dysfunction and behavioral abnormalities

doi: 10.1038/s41380-020-0671-2

Figure Lengend Snippet: a Gene ontology (GO) biological processes pathway analysis shows that MIA microglia increase synaptogenic functions while repopulated microglia recover homeostatic functions. Left (red): Top significantly enriched GO biological process terms increased by MIA and decreased by repopulation. Right (purple): Top significantly enriched GO biological process terms decreased by MIA and increased by repopulation. These GO findings were verified using GORILLA. b IPA of genes with differential expression in microglia between MIA versus Saline (RNA-seq data). Pathway analysis reveals MIA-induced upregulation of neuritogenic gene expression, specifically in developmental stages, based on activation z -score. Red denotes pathway activated in E17 MIA microglia. c Genes in “neuritogenesis/formation of cellular protrusions” function. Hierarchal clustering of gene sets based on relative expression values; red: high relative expression, blue: low relative expression. Cluster 1 represents genes increased in adult MIA microglia but reduced in MIA + MG-REP including Ctnnd2, Ncam2, and Ntrk2 . Cluster 2 represents genes increased in immature MIA microglia including Ncam2, Ntn, Ptn and Wnt5a . Cluster3 represents genes decreased in immature MIA microglia including Plau. In situ hybridization (ISH) and immunofluorescence of E17 Saline or MIA offspring in the cortical plate region. d mRNA of cellular protrusion/ neuritogenic genes ( Ctnnd2, Ncam2, Ntn, Ptn, and Wnt5a ) were detected by florescent-labeled antisense cRNA probes (red) but not by scramble cRNA probe (not detected: N.D.), and the sections were immunostained for IBA1 (green) and DAPI (blue). e The number of IBA1 + cells expressing the cellular protrusion/neuritogenic genes were quantified in the cortical plate region. n = (4–5/2) male mice/ litters per molecule for Saline and MIA, n = 3 for scramble control probe. * p < 0.05, ** p < 0.01, ns denotes no significance, by unpaired Student t test. Graphs indicate mean ± s.e.m. ELISA verification of selected RNA-seq molecules: CTNND2 ( f ), NCAM2 ( g ), NTRK2 ( h ), NTN ( i) , PTN ( j ) and WNT5A ( k ) in acutely isolated microglia. MIA increases protein expression of cellular protrusion/neuriotgenic molecules in microglia that were normalized via repopulation. n = (6/4, 6/3, 5/3, 6/3) female mice/litters for P60 Saline + CTRL, MIA + CTRL, Saline + MG-REP and MIA + MG-REP. CTNND2: Prenatal treatment effect, F (1,19) = 157.1, p < 0.0001, Drug effect, F (1,19) = 262.7, p < 0.0001, Interaction effect, F (1,19) = 201, p < 0.0001, NCAM2: Prenatal treatment effect, F (1,19) = 23.76, p = 0.0001, Drug effect, F (1,19) = 26.29, p < 0.0001, Interaction effect, F (1,19) = 17.63, p = 0.0005, NTRK2: Prenatal treatment effect, F (1,18) = 13.99, p = 0.0015, Drug effect, F (1,18) = 12.45, p = 0.0024, Interaction effect, F (1,18) = 0.06203, p = 0.8061, NTN: Prenatal treatment effect, F (1,19) = 0.01669, p = 0.8986, Drug effect, F (1,19) = 0.8, p = 0.3823, Interaction effect, F (1,19) = 6.121, p = 0.0230, PTN: Prenatal treatment effect, F (1,19) = 10.31, p = 0.0046, Drug effect, F (1,19) = 52.02, p < 0.0001, Interaction effect, F (1,19) = 0.002927 p = 0.9574, WNT5A: Prenatal treatment effect, F (1,19) = 5.581, p = 0.0290, Drug effect, F (1,19) = 1.550, p = 0.2282, Interaction effect, F (1,19) = 0.0834 p = 0.7799, * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 as determined by 2-way ANOVA (alpha = 0.05) with Tukey’s post-hoc. # p < 0.05 for main effect of MIA. Graphs indicate mean ± s.e.m.

Article Snippet: For the detection of NTRK2 (TrkB), PTN and NTN1, following commercial ELISA kits were used: Mouse TrkB ELISA kit (Boster Biological Technology, EK0849), Mouse PTN ELISA kit (Biomatik Corporation, EKU06717), Mouse NTN1 ELISA kit (LifeSpan Biosciences, LS-F5882).

Techniques: Quantitative Proteomics, Saline, RNA Sequencing, Gene Expression, Activation Assay, Expressing, In Situ Hybridization, Immunofluorescence, Labeling, Control, Enzyme-linked Immunosorbent Assay, Isolation